Osteopenia antibiotics, a cause of bone loss and osteoporosis?

Osteopenia antibiotics.The list of things that cause Osteopenia and Osteoporosis could include antibiotics.... or maybe not.

As early as 2006 there were some reports in the media that
long term use of antibiotics can be a cause of Osteoporosis or
Osteopenia. If true, then persons taking antibiotics for a month
or more, should speak with their health care provider about diagnostic
monitoring and/or supplements to counteract the effects of the
antibiotics on their bones.

The U.S. National Institutes
of Health digital archive of biomedical and life sciences journal
literature, contains very few studies concerning Osteoporosis Osteopenia antibiotics connection. cause

There is one study from Poland about a male patient with lyme disease who took Vibramacin for a
month. The author of the study was Hrycek A, Oslawska-Dierzega A,
Kossowski M, Kasztura W. The abstract stated that:

"A male patient aged 38 was complaining from severe musculo-arthral
pains and high body temperature of 39 degrees C. He was admitted to the
clinical hospital after long and detailed diagnostic
procedures--conducted during previous hospitalization, which focused on
Plasmocytoma. Serological examinations relating to Lyme disease were
undertaken in the clinical hospital and the results appeared positive.
The patient received Vibramicin for a prolonged treatment lasting 30
days. Radiological findings showed distraction in both hip joints
(especially the right one), with areas of bone erosion, severe
osteoporosis and calcifications in periarthral soft tissues. After
pharmacological treatment the body temperature normalized and the pain
became less severe. The state of the patient's health improved from
subjective and objective point of view."

The other side: Osteoporois, Osteopenia antibiotic as helpful medication.

However, there are also other studies that indicate that antibiotics are NOT a cause of Osteopenia or Osteoporosis. Instead they might be useful in the treatment of bone loss!

They
performed the study to test the Effect of minocycline on osteoporosis
and they used ovariectomized (OVX) old rats. The subjects were treated
with Minocycline as a way to reduce bone resorption [bone removal] and
to stimulate the formation of new bone. The study found that: that
oral minocycline can effectively prevent the decrease in BMD and
trabecular bone through its dual effects on bone resorption and
formation.

In particular the study found that "the loss of
trabecular connectivity was prevented by treatment with minocycline or
estrogen". They said:

"Based on the levels of urinary
pyridinoline, we showed that the effect of estrogen, but not
minocycline, was primarily through its inhibitory effect on bone
resorption. Analysis of bone turnover activity suggests that OVX
increased parameters associated with bone resorption (eroded surface)
and formation (osteoid surface, mineralizing surface, mineral
apposition rate, and bone formation rate). Treatment with minocycline
reduced bone resorption modestly and stimulated bone formation
substantially. In contrast, treatment with estrogen drastically reduced
parameters associated with both bone resorption and formation."

Another study done in 1991 showed that Tetracycline administration
restores osteoblast structure and function during experimental diabetes.
This study was done by Sasaki T, Kaneko H, Ramamurthy NS, Golub
LM. from the Second Department of Oral Anatomy, School of Dentistry,
Showa University, Tokyo, Japan.

Their abstract states:

"Osteopenia
is a recognized complication of diabetes mellitus in humans and
experimental animals. We recently found that tetracyclines prevent
osteopenia in the streptozotocin-induced diabetic rat and that this
effect was associated with a restoration of defective osteoblast
morphology (Golub et al., 1990). The present study extends these initial
ultrastructural observations by assessing osteoblast function in the
untreated and tetracycline-treated diabetic rats.

After a 3-week
protocol, non-diabetic control and diabetic rats, including those
orally administered a tetracycline, minocycline (MC), or a
non-antimicrobial tetracycline analog (CMT), were perfusion-fixed with
an aldehyde mixture; the humeri were dissected and processed for
ultracytochemical localization of alkaline phosphatase (ALPase) and
Ca-ATPase activities. Some rats from each experimental group received
an intravenous injection of 3H-proline as a radioprecursor of
procollagen, and the humeri were processed for light microscopic
autoradiography. In addition, the osteoid volume in each experimental
group was quantitatively examined by morphometric analysis of electron
micrographs.

During the diabetic state, active cuboidal
osteoblasts in the endosteum of control rats were replaced by flattened
bone-lining cells that contained few cytoplasmic organelles for protein
synthesis (Golgi-RER system), and active transport (mitochondria).
Treating diabetic rats with MC, and even more so with CMT, appeared to
"restore" osteoblast structure. During diabetes, bone-lining cells
incorporated little 3H-proline or secreted little labeled protein and
produced only a very thin osteoid layer. Tetracycline administration to
the diabetics increased both the incorporation of 3H-proline by
osteoblasts and their secretion of labeled protein toward the osteoid
matrix, in a pattern similar to that seen in the non-diabetic
controls."

So are antibiotics a cause of Osteopenia or are they a potential treatment?
It appears that the jury is still out on this one. But if you are
having a long treatment with antibiotics, it might be useful to ask you
health care provider to monitor your bone mineral density since at least
some scientists think there may be an antibiotic osteopenia, osteoporosis link.